Microbiota-host interactions in irritable bowel syndrome: Epithelial barrier, immune regulation and brain-gut interactions

Abstract

Irritable bowel syndrome (IBS) is a common, sometimes debilitating, gastrointestinal disorder worldwide. While altered gut motility and sensation, as well as aberrant brain perception of visceral events, are thought to contribute to the genesis of symptoms in IBS, a search for an underlying aetiology has, to date, proven unsuccessful. Recently, attention has been focused on the microbiota as a possible factor in the pathogenesis of IBS. Prompted by a number of clinical observations, such as the recognition of the de novo development of IBS following enteric infections, as well as descriptions of changes in colonic bacterial populations in IBS and supported by clinical responses to interventions, such as antibiotics and probiotics, that modify the microbiota, various approaches have been taken to investigating the microbiota-host response in IBS, as well as in animal models thereof. From such studies a considerable body of evidence has accumulated to indicate the activation or upregulation of both factors involved in bacterial engagement with the host as well host defence mechanisms against bacteria. Alterations in gut barrier function, occurring in response, or in parallel, to changes in the microbiota, have also been widely described and can be seen to play a pivotal role in generating and sustaining host immune responses both within and beyond the gut. In this manner a plausible hypothesis, based on an altered microbiota and/or an aberrant host response, for the pathogenesis, of at least some instances of IBS, can be generated.

Keywords: Microbiota, Irritable bowel syndrome, Toll-like receptor, Epithelial barrier, Gut-brain axis

Core tip: Recent discoveries have kindled an interest in microbiota-host interactions in irritable bowel syndrome (IBS) and have led to new lines of research into this common and elusive disorder. It is clear that the microbiota is altered in IBS and that such alterations could well contribute to the pathogenesis of the disorder through, for example, increased permeability, an altered immune profile, effects on the central nervous system and modulation of gut neuromuscular function. This review will explore these host-microbe interactions and their relevance to the pathogenesis of IBS. This review will explore these interactions and their relevance to the pathogenesis of IBS.